A 59-year-old female presents to the emergency department with a chief complaint of “head pain that comes and goes.”

She describes the pain as a dull ache in her occiput that’s been striking without warning a couple of times per day for the past ten days. Over the last three days she’s noted that it has also been radiating into her neck and upper back/shoulders.

Because of her vague symptoms and pain that involves her back/shoulders, a 12-lead ECG is performed soon after arrival.

For the rest of this case description please follow this link or click on the ECG above.

A 22-year-old male presents with agitation and delirium after smoking an unknown substance that an equally unknown person on the street offered him. You note a rapid radial pulse at around 150 bpm and attach him to the cardiac monitor:

Figure 1. Initial rhythm at normal paper speed (25 mm/s).

Well now we’re in a tough spot. It’s difficult to tell whether Fig. 1 shows sinus tachycardia or some non-sinus narrow-complex tachycardia (we’ll use the colloquial shorthand of “SVT” to include all those other options on the differential, including AVNRT, AVRT, ectopic atrial tachycardia, junctional tachycardia, etc…). If it is indeed sinus tach, then the requisite P-waves must be those upright deflections in II and III and superimposed on the T-waves.

Is there something we could do to see if those really are P-waves buried in the T-waves?

If you’re like me, you were probably taught that it would be a clever move to double the paper speed in a situation like this to separate the P’s from the T’s, revealing the diagnosis of sinus tachycardia. Let’s see what happens when we do that.

For the rest of this case and discussion please follow this link or click on the rhythm strip above.

This article is the ninth in our latest series, The 12 Rhythms of Christmas, where we examine a different rhythm disorder with each new post. It’s a continuation of the theme behind last year’s 12 Leads of Christmas. And, just like last year’s series, I’m rather late getting the final articles out, but the end is in sight.

Hope you had a good Valentine’s Day—let’s talk about some heart stuff. Today I want to discuss a form of AV-block that many providers don’t even realize is its own unique entity: paroxysmal AV-block.

What differentiates this arrhythmia from the other AV-blocks is that it occurs in discrete, self-limited episodes—or “paroxysms.” You patient will be hanging out, minding their own business, when out of nowhere they suddenly drop two or three or forty QRS complexes in a row until the AV-node just as suddenly recovers. It tends to give you a pretty good wake-up.

High-grade AV-block (sometimes called advanced AV-block) is how we describe a form of pathological AV-block where two or more consecutive P-waves fail to conduct to the ventricles.

Why don’t we just call the tracing in Fig. 4 type II AV-block? Think back to the basis of our article on 2:1 AV-block: Since we never see two P-waves in a row that conduct, we cannot assess whether the PR-interval is progressively increasing (as in type I AV-block) or fixed (as in type II AV-block). You might think that all high-grade AV-blocks must be due to a type II mechanism because the conduction defect looks so severe, but even type I AV-blocks can exhibit the sort of behavior we see above. In fact, based on subsequent tracings (not shown here), there’s a pretty decent chance both the patients whose rhythms we’re going to examine in this post were experiencing high-grade AV-block due to an underlying type I mechanism.

For the rest of this discussion please follow this link or click on the rhythm strip above.

Our last two posts have examined type I and type II AV-block, so it’s only fitting that we continue our theme with a topic that combines the two:

While most everyone has heard of first degree, type I, type II, and complete AV-block, comparatively few people recognize 2:1 AV-block as a valid rhythm diagnosis in its own right. That’s a shame, because 2:1 AV-block is a rather interesting finding. To understand why, consider the following dilemma:

Type I AV-block presents with progressively increasing PR-intervals until a P-wave is blocked

Figure 1. Increasing PR-intervals in the setting of type I AV-block. Measurements are in milliseconds.

Type II AV-block presents with fixed PR-intervals until a P-wave is blocked

It should be clear from the two examples above (and the others in this series) that both forms of AV-block can present with various—and actively varying—conduction ratios: 5:4, 4:3, 3:2, etc… That doesn’t affect our ability to diagnose the rhythms, and in fact, it can be helpful to see how the PR-intervals behave with different ratios of P-waves to QRS-complexes.

What do you do, however, when every-other P-wave is blocked?

Figure 3. 2:1 AV-block of uncertain mechanism.

For the rest of this discussion please follow this link or click on the rhythm strips above.

Type I AV-block is a pretty interesting phenomenon, first described in 1899 by Dutch anatomist Karel Wenckebach. It is characterized by progressive lengthening of the PR-intervals that culminates in a dropped (fully blocked) P-wave and a pause in the ventricular rhythm, reseting the AV-node so that the cycle can repeat.

Let’s look at an example:

Even those with limited experience in basic dysrhythmias should be able to identify the increasing PR-intervals…

That, however, is where most folks’ knowledge ends. But I expect most of the folks reading this blog, if they don’t already, would like to understand why this pattern occurs.

For the rest of this article please follow this link or click the rhythm strips above.

This is a new edit of the first article I ever published on this blog, so it may seem familiar to some readers.

Have you slammed adenosine to cure a patient’s SVT with a fluorish?

Figure 1. Pre-adenosine.

*PUSH* – *FLUSH* – “You’re gonna feel funny.”

Figure 2. A few seconds after the adenosine push.

…only to see the saw-tooth waves of atrial flutter marching across the monitor?

While you may have performed a successful diagnostic test, your unsuspecting patient has just been given a sneak peek of the day their heart quits beating with no relief from the arrhythmia actually causing their symptoms.

Well, you need-not make that mistake again, because I’ve put together a rough list of (almost) every tip out there for diagnosing subtle atrial-flutter with 2:1 conduction. In the end you’ll be talented enough to recognize this arrhythmia with your monitor upside-down (hint)!

For the rest of this article please follow this link or click on the rhythm strips above.

Last year I posted a nearly identical article titled Don’t let your bradycardic patient D.I.E., but this is an update focused on sinus bradycardia and with a slightly new mnemonic. Our new post should be called, Don’t let the cause of bradycardia H.I.D.E..

I’ve told you before that I’m terrible with mnemonics, but there is one I used to find both memorable and useful: the DIE mnemonic for insidious but reversible causes of bradycardia in the emergency medicine and acute care setting. DIE stands for drugs, ischemia, electrolytes. While I love its simplicity, I no longer rely on that exact mnemonic because it leaves out an important cause of bradycardia you do not want to miss—hypothyroidism.

Unlike ischemia, hypothyroidism is not a major concern from a prehospital perspective, and unlike hyperkalemia, it’s not quickly reversible, but given its importance in the trajectory of a patient’s care and how easily it can be overlooked, I think it still deserves a spot in my favorite memory aid.

[H]ypothyroidism
[I]schemia
[D]rugs
[E]lectrolytes

Yes, there are other causes of bradycardia that should be on your differential, but what makes this list special is that all four have specific emergency treatments, the standard ACLS trio of pacing, atropine, and dopamine/norepi does little or nothing to address them, and, if missed, patients are unlikely to get better with only supportive care.

For the rest of this article please follow this link or click on the ECG below.